Angeles University Foundation

Angeles City

Case Analysis

Group 1

BSMT 3A

DIMLA, Mary Kimberly

PARTOLAN, Mark Jadrian
SALINAS, March Tracy
TORRES, Kristensen

January 7, 2010

CASE 2

From a rural hospital in Barangay Ilang-Ilang, this 71-year old woman was transferred to a tertiary hospital
complaining of shortness of breath and showing evidence of pulmonary edema. There was no history of chest
pains, nausea, vomiting or diaphoresis. Her admission diagnosis was Congestive Heart failure (acute exacerbation),
Myocardial Infarction (subendocardial), DM and HTN. Medications included Lasix, morphine, nitroglycerin, and
Procardia. Laboratory tests were significant for increased CK, 544 U/L (21-215) with a CKMB of 29.2 ng/mL (0-4),
which is a relative index of 54. During the first few days of her hospital stay, blood glucose ranged from 201 to 365
mg/dL (70-110); creatinine ranged from 1.9 to 3.7 mg/dL (0.6-1.0); and BUN ranged from 31 to 46 mg/dL (5-25).
Admission urinalysis was significant for: glucose 100 mg/dL; blood moderate; protein >300 mg/dL (<90); WBCs 2-
5/hpf; RBCs 10-20/hpf; epithelials/lpf few squamous, few renal; casts/lpf 5-10 granular, 0-1 WBC. After aggressive
treatment of the she received intravenous nitroglycerin and insulin. The discharge diagnosis was status
postsubendocardial MI, triple-vessel cardiac disease, CHF, renal insufficiency, HTN, and DM. She was scheduled to
return to the hospital eventually for a triple vessel coronary bypass. What renal condition do the urinalysis data
suggest? Explain. Do the analyses on blood correlate with this? Explain. What is the pathophysiology behind the
renal condition in the first question? Explain.

Gender: Female
Age: 71

Symptoms:

Shortness of breath
Pulmonary edema

*no chest pains

*no nausea
*no vomiting

Diagnosis:

CHF (Congestive Heart Failure)

MI (Myocardial Infarction)
HTN (Hypertension)
DM (Diabetes Mellitus)

Medications:
Lasix – CHF
Morphine –pain killer
Nitroglycerin –vasodilator
Procardia –antiaginal, antihypertensive
Insulin –DM

Blood Chemistry Results:

CK -554u/l
CKMB -29.2u/L
Glucose - 201 to 365 mg/dL (70-110)
Creatinine- 1.9 to 3.7 mg/dL (0.6-1.0)
BUN- 31 to 46 mg/dL (5-25)

Urinalysis Results:

Chemical:
Glucose: 100mg/dl
Blood (moderate)
Protein- >300 mg/dL (<90)

Microscopic:
RBC 10-20/hpf
WBC 2-5/hpfb
Epithelial. Cells (few)
Renal Cell (few)
Granular Cast (5-10/lpf)
Leukocyte Casts (0-1/lpf)

Patient Diagnosis:

Chronic Glomerulonephritis
Terminologies

Cardiac markers (CKMB) are biomarkers measured to evaluate heart function. They are often discussed in the
context of myocardial infarction, but other conditions can lead to an elevation in cardiac marker level.

Blood urea nitrogen (BUN) test is a measure of the amount of nitrogen in the blood in the form of urea, and a
measurement of renal function.

Pulmonary edema is fluid accumulation in the lungs. It leads to impaired gas exchange and may cause respiratory
failure.

Congestive Heart failure (CHF) is a condition in which a problem with the structure or function of the heart impairs
its ability to supply sufficient blood flow to meet the body's needs. The phrase is often wrongly used to describe
other cardiac-related illnesses, such as myocardial infarction (heart attack) or cardiac arrest.
Hypertension is a chronic medical condition in which the blood pressure is elevated. It is also referred to as high
blood pressure or shortened to HT, HTN or HPN. The word "hypertension", by itself, normally refers to systemic,
arterial hypertension.

Diabetes mellitus often referred to as diabetes—is a condition in which the body either does not produce enough,
or does not properly respond to, insulin, a hormone produced in the pancreas.

Furosemide (INN) or frusemide (former BAN) is a loop diuretic used in the treatment of congestive heart failure
and edema. It is most commonly marketed by Sanofi-Aventis under the brand name Lasix.

Morphine is an extremely potent opiate analgesic psychoactive drug, is the principal active ingredient in Papaver
somniferum, is considered to be the prototypical opioid. In clinical medicine, morphine is regarded as the gold
standard, or benchmark, of analgesics used to relieve severe or agonizing pain and suffering.

Nitroglycerin is also used medically as a vasodilator to treat heart conditions, such as angina and chronic heart
failure.

Nifedipine (brand name Adalat, Nifedical, and Procardia) is a dihydropyridine calcium channel blocker. Its main
uses are as an antianginal (especially in Prinzmetal's angina) and antihypertensive,

Guide Questions:

What renal condition do the urinalysis data suggest? Explain. Do the analyses on blood correlate with this?
Explain. What is the pathophysiology behind the renal condition in the first question? Explain.

CHRONIC GLOMERULONEPHRITIS. Based on the urinalysis test results of the patient, there is a high elevation of
protein (proteinuria) and glucose level, a moderate amount of blood (hematuria) has been also detected
accompanied by granular and cellular cast. in which these findings are assumed to be the primary urinalysis test
result of this renal condition.

YES it correlates. According to the blood test assessment, the level of Blood Nitrogen Urea (BUN) and creatinine
are markedly increased, this may result to a decreased glomerular filtration rate. When GFR is impaired, less
creatinine is excreted by the glomerulus causing serum levels to rise. While the concentration of urea nitrogen in
the blood reflects glomerular filtration and urine-concentrating capacity. Because urea is filtered at the
glomerulus, blood urea nitrogen (BUN) levels increase as glomerular filtra-tion drops. Because urea is reabsorbed
by the blood through the permeable tubules, the BUN rises in states of dehydration and acute and chronic renal
failure when passage of fluid through the tubules is slowed. BUN also varies because of altered protein intake and
protein catabolism and therefore is a poor measure of GFR. The application of this principle is useful for
monitoring progressive changes in renal function. Serum creatinine and BUN are elevated in chronic
glomerulonephritis and other related renal conditions.

PATHOPHYSIOLOGY OF CHRONIC GLOMERULONEPHRITIS:

Chronic glomerulonephritis occurs when there is slow, progressive destruction of the glomeruli of the kidney, with
progressive loss of kidney function. Damage to the glomeruli affects the kidney's ability to filter fluids and wastes
properly. This leads to blood and protein in the urine called microscopic hematuria and proteinuria. The
inflammation causes blood and protein to leak into the urine. As protein levels in the blood fall, excess fluid
accumulates in the body.
Tests show protein, blood cells, and kidney cells in the urine, while a high concentration of the body's waste
products of metabolism (such as urea and creatinine) may be found in the blood.

Creatinine is a substance that is produced by muscle and released into the blood at a relatively constant rate.
Laboratory tests for serum creatinine provide an indicator or glomerular filtration rate (GFR). When the GFR is
damaged a reduced amount of creatinine is being emit by the the glomerulus that causes the serum creatinine
levels to increase.

BUN reflects the GFR, because the urea is being filtered to glomerulus, when the BUN elevates the GFR drops,
because the urea is being reabsorbed by the blood through the permeable tubules, the BUN rises in chronic renal
failure when passage of fluid through the tubules is slowed. BUN also varies because of altered protein intake and
protein catabolism and therefore is a poor measure of GFR.

Casts (accumulations of cellular precipitates) originate in the renal tubules, from which they take their shape. They
are cylindrical with distinct borders. All casts have a precipitated microprotein matrix and arise primarily from the
ascending limb of the distal tubule. Granular Cast, indicates that the patient occur glomerulonephritis. The type of
cast identified suggests the disease process occurring in the kidney.

White blood cells (WBCs) in the urine (a condition termed pyuria) are primarily indicative of urinary tract infection,
particularly when bacteria are present. Glomerulonephritis and nephrotic syndrome also may demonstrate pyuria,
but usually in combination with proteinuria, red cells, and casts. The finding of WBC casts reflects a kidney
infection, because these casts are not formed in the bladder or prostate.

Chronic glomerulonephritis usually causes only very mild or subtle symptoms, it goes undetected for a long time in
most people. Edema may occur. High blood pressure is common. The disease may progress to kidney failure, which
can cause itchiness, fatigue, decreased appetite, nausea, vomiting, and difficulty breathing.
Questions

Which of the following is not a symptom of Chronic Glomerulonephritis

hypertension
edema
oliguria
hypotension

All are types of immune mechanisms which contributes to glomerular injury except:
a. Deposition of circulating soluble antigen-antibody complexes
b. Formation of antibodies specific against the glomerular basement membrane
c. Streptococcal release of neuramidase, which alters IgG with binding of anti-IgG to the
glomerulus.
d. none of the above

Chronic Glomerulonephritis includes primary urinalysis results except:

a. hematuria
b. proteinuria
c. granular cast
d. oval fat bodies

Other significant test for Chronic Glomerulonephritis includes:

serum creatinine
creatinine clearance
both a and b
none of the above
Reduction in nephron mass from the initial injury reduces the GFR then leads to:
hypertrophy
hyperfiltration of the remaining nephrons
both a and b
none of the above

Which of the following best describes Chronic Glomerulonephritis:

Occurs primarily in children following viral respiratory infections.
Disruption of podocutes in certain areas of glomeruli associated with heroin and analgesic abuse.
Deposition of IgA on the glomerular membrane resulting from increased levels of serum IgA
Marked decrease in renal function resulting from glomerular damage precipitated by other renal disorder.

Which of the following is not a cause of Chronic glomerular injury:

Insulin-dependent diabetes mellitus
lupus erythematosus
Hypercholesterolemia
None of the above

Chronic Glomerulonephritis can be caused by:

mercury
non-steroidal anti-inflammatory analgesics
HIV
All of the above

First indicator of renal disorder is:

protein
glucose
blood
abnormal sediment

The most significant and the only one that can be found in a cast:
WBC
RBC
Renal epithelial
Squamous epithelial

Chronic glomerulonephritis

Chronic glomerulonephritis is the advanced stage of a group of kidney disorders, resulting in inflammation and
slowly worsening destruction of internal kidney structures called glomeruli.
Causes, incidence, and risk factors:

Chronic glomerulonephritis occurs when there is slow, progressive destruction of the glomeruli of the kidney, with
progressive loss of kidney function. In some cases, the cause is found to be a specific attack to the body's immune
system, but in most cases, the cause is unknown. Iit is generally thought that a still-unidentified abnormality of the
immune system is to blame.

Damage to the glomeruli affects the kidney's ability to filter fluids and wastes properly. This leads to blood and
protein in the urine.
This condition may develop after survival of the acute phase of rapidly progressive glomerulonephritis. In about
one-quarter of people with chronic glomerulonephritis there is no prior history of kidney disease, and the disorder
first appears as chronic kidney failure.

Glomerulonephritis is among the leading causes of chronic kidney failure and end stage kidney disease. Causes
include:

* Diabetic nephropathy/sclerosis
* Focal segmental glomerulosclerosis
* IgA nephropathy (Berger's disease)
* Lupus nephritis
* Membranous glomerulonephritis
* Mesangial proliferative disorder
* Nephritis associated with disorders such as amyloidosis, multiple myeloma, or immune disorders, including
AIDS

Symptoms:

This condition causes high blood pressure (hypertension) and chronic kidney failure.

Specific symptoms include:

* Blood in the urine (dark, rust-colored, or brown urine)

* Foamy urine

Chronic kidney failure symptoms that gradually develop may include the following:

* Decreased alertness
o Drowsiness, somnolence, lethargy
o Confusion, delirium
o Coma
* Decreased sensation in the hands, feet, or other areas
* Decreased urine output
* Easy bruising or bleeding
* Fatigue
* Frequent hiccups
* General ill feeling (malaise)
* Generalized itching
* Headache
* Increased skin pigmentation -- skin may appear yellow or brown
* Muscle cramps
* Muscle twitching
* Nausea and vomiting
* Need to urinate at night
* Seizures
* Unintentional weight loss

Additional symptoms that may be associated with this disease:

* Blood in the vomit or stools

* Excessive urination
* High blood pressure
* Nosebleed
Signs and tests:

Because symptoms develop gradually, the disorder may be discovered when there is an abnormal urinalysis during
a routine physical or during an examination for another, unrelated disorder. It may be discovered as a cause of
high blood pressure that is difficult to control.

Laboratory tests may reveal anemia or show signs of reduced kidney functioning, including azotemia. Later, signs
of chronic kidney failure may be apparent, including edema .

Tests that may be done include:

* Chest x-ray
* Kidney or abdominal CT scan
* Kidney or abdominal ultrasound
* IVP
* Urinalysis

A kidney biopsy may show one of the forms of chronic glomerulonephritis or scarring of the glomeruli.

This disease may also alter the results of the following tests:

* Albumin
* Abdominal MRI
* Anti-glomerular basement membrane
* BUN
* Complement component 3
* Complement
* Creatinine clearance
* Renal scan
* Total protein
* Uric acid, urine
* Urine concentration test
* Urine creatinine
* Urine RBC
* Urine specific gravity
* Urine protein

Treatment:

Treatment varies depending on the cause of the disorder, and the type and severity of symptoms. The primary
treatment goal is control of symptoms. High blood pressure may be difficult to control, and it is generally the most
important aspect of treatment. Various medications may be used to attempt to control high blood pressure.

Corticosteroids, immunosuppressives, or other medications may be used to treat some of the causes of chronic
glomerulonephritis.

Dietary restrictions on salt, fluids, protein, and other substances may be recommended to help control of high
blood pressure or kidney failure.

Dialysis or kidney transplantation may be necessary to control symptoms of kidney failure and to sustain life.

The outcome varies depending on the cause. Some types of glomerulonephritis may get better on their own.
If nephrotic syndrome is present and can be controlled, other symptoms may be controlled. If nephrotic syndrome
is present and cannot be controlled, end-stage kidney disease is likely.

The disorder worsens at widely variable rates.

Complications:

* Nephrotic syndrome
* Acute nephritic syndrome
* Chronic renal failure
* End-stage renal disease
* Hypertension
* Malignant hypertension
* Fluid overload -- congestive heart failure, pulmonary edema
* Chronic or recurrent urinary tract infection
* Increased susceptibility to other infections

I. SUMMARY OF THE CASE

The 49 year old male presented in E.R. was complaining of abdominal pain accompanied by nausea, vomiting,
some coughing which is non-productive and a slightly erythematous rash on the toes of both feet. He was
experiencing these in the past 5 months and was getting worst in the last two days. The patient medical history
show the he was diagnosed with AIDS last year, disseminated tuberculosis and was an intravenous drug abuser. On
admission, the patient is taking in some medications and this includes:
 INH (Isonicotinic Acid Hydrazide) - It is prescribed for prophylaxis for those who have been exposed to
tuberculosis and is used in combination with other agents in the treatment of tuberculosis caused by
mycobacteria sensitive to the drug. Adverse effect: Rashes
 RIFAMPIN - an antituberculosis agent, it works by killing or stopping the growth of tuberculosis bacteria.
Adverse effects: reddish orange discoloration of body fluids including urine,
 BACTRIM DS – antibiotic that treat different types of infection caused by bacteria, used to treat ear
infections, urinary tract infections, bronchitis, traveler's diarrhea, and Pneumocystis carinii pneumonia.
Adverse effects: nausea, vomiting, abdominal pain and allergic skin reactions such as rash and urticaria,
Cough and pulmonary infiltrates
 He is also taking in Megace, Flucon, MS Contin, Morphine Elixir

The patient’s abdomen x-ray showed multiple air- fluid levels in the small bowel. The patient was then admitted
for observation and treatment of the ileus. The results Urinalysis are as follows:
 Color- amber
 pH- 7.0
 Specific Gravity- 0.020
 Glucose- negative
 Bilirubin- negative
 Ketone- negative
 Blood- negative
 Nitrite and leukocyte esterase- negative
 Urobilinogen- normal
 Protein- 30mg/dl

He was discharged after 3 days in stable condition and continued taking in Bactrim DS, INH, Rifampin and Diflucan.

II. ANSWER TO GUIDE QUESTIONS

1. Are there any significant findings in the urinalysis?

 Yes, the positive urine protein may indicate a renal disease. The result of the Urinalysis of the patient
is 30mg/dL which is trace to 1+. Normal urine contains very little protein; usually, less than 10mg/dL
or 100mg/24 hours is excreted and clinical proteinuria is indicated at >30mg/dL.

2. How would you characterize the casts and cells that may be observed in the urine if microscopic analysis
was performed?
Hyaline casts may appear + sulphonamide crystals due to administration of Bactrim.

3. What pathophysiologic picture is illustrated by the urinalysis in this case?

This is a possible case of Focal Segmental Gloerulosclerosis, secondary to narcotic abuse. The
patient’s urine protein which is 30mg/dL is considered normal since clinical proteinuria is indicated at
>30mg/dL of urine protein, but it still depends upon the severity of the disease. We have concluded
that this is a possible case of FSGS probably because the disseminated tuberculosis of the patient was
just starting to affect the urinary system that is why only trace up to 1+ protein is present.
AMBER COLORED URINE is due to Rifampin, while nausea, vomiting, abdominal pain and allergic
skin reactions such as rash and urticaria are the most common adverse effects of Bactrim DS
associated with the Gastrointestinal Tract. Cough and pulmonary infiltrates are also adverse effect of
Bactrim DS related with Respiratory. Side effects generally are more common and more severe in
patients with AIDS. Side effects generally are more common and more severe in patients with AIDS.
Hypersensitivity reactions may be more likely in patients with HIV infection, with opportunistic
infections.
ILEUS; an obstruction of the intestine can cause ABDOMINAL PAIN due to contractions of intestinal
muscle and distension of intestine. This Abdominal Pain may worsen due to COUGHING. Patients with
ILEUS may also report NAUSEA AND VOMITING. One probable cause of ileus is the USE OF CERTAIN
DRUGS, such as NARCOTIC PAIN DRUGS or high blood pressure medicine.
DISSEMINATED TUBERCULOSIS (TB) is a contagious bacterial infection that has spread from the lungs
to other parts of the body through the blood or lymph system. Disseminated disease develops in the
small number of infected people whose immune systems do not successfully contain the primary
infection. Since the patient was diagnosed with ADIS, therefore he is immune compromised.

III. SAMPLE TEST PAPER

1. This is the most indicative of renal disease among the routine chemical tests performed on urine:
a) Protein c) pH
b) Glucose d) Blood

2. Normal levels of protein present in urine daily:

a) 5mg/dL c) 15mg/dL
b) 10mg/dL d) 20mg/dL

3. The amber color urine was caused by which of the following medications that the patient is taking in?
a) INH c) Rifampin
b) Bactrim DS d) Flucon

4. With the given Physical and Chemical results, Microscopic Analysis should be requested.
a) Statement is TRUE
b) Statement is FALSE

5. What Renal disorder is related to the case of the patient?

a) Acute Glumerulonephritis c) Alport Syndrome
b) Focal Segmental d) Good Pasture Syndrome
Glomerulosclerosis
 6. Among which of the following Renal Disease may resemble with your answer in number 5?
a) Nephrotic Syndrome c) Either
b) Minimal Change Disease d) Neither

7. Focal Segmental Glomerulosclerosis is often associated with the following conditions seen in the patient
except:
a) Cough c) Narcotic abuse of drugs
b) AIDS d) NIL

8. What are the cast or cells that may be present if Microscopic Analysis is performed?
a) Fatty Cast
b) Hyaline Cast
c) Waxy Cast
d) RBC Cast

9. The cause of proteinuria based on the origin of Protein:

a) Pre renal c) Post Renal
b) Renal d) NIL

10. Clinical proteinuria is indicated in which of the following protein levels in urine?
a) >10mg/dL c) >30mg/dL
b) >20mg/dL d) >40mg/dL

ANSWERS:
1. A) Protein
2. B) 10mg/dL
3. C) Rifampin
4. A) TRUE
5. B) Focal Segmental Glomerulosclerosis
6. C) Either
7. A) Cough
8. B) Hyaline Cast
9. B) Renal
10. B) >30mg/dL

IV. PERTINENT INFORMATION

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

FSGS affects only certain numbers and areas of glomeruli, and others remain normal. Symptoms may be similar to
the nephritic syndrome and minimal change disease owing to damaged podocytes. Immune deposits, primarily
immunoglobulins M and C3, are a frequent finding and can be seen in undamaged glomeruli. FSGS is often seen in
association with abuse of heroin and analgesics and with AIDS. Moderate to heavy proteinuria and microscopic
hematuria are most consistent urinalysis findings.
Focal Segmental Glomerulosclerosis is a disease that attacks the kidney’s filtering system (glomeruli) causing
serious scarring. FSGS affects only certain numbers and areas of glomeruli, and others remain normal. Symptoms
may be similar to the nephritic syndrome and minimal change disease owing to damaged podocytes. FSGS is often
seen in association with abuse of heroin and analgesics and with AIDS. Moderate to heavy proteinuria and
microscopic hematuria are most consistent urinalysis findings.
Primary UA results:
Proteinuria
Microscopic hematuria
Macroscopic or microscopic hematuria

Other Significant test:

Drugs of abuse
HIV tests
Genetic testing
Etiology:
Disruption of podocytes in certain areas of glomeruli associated with heroin and analgesic abuse and AIDS.

Clinical course:
May resemble nephritic syndrome or minimal change disease

The individual components of the name refer to the appearance of the kidney tissue on biopsy: FOCAL—only some
of the glomeruli are involved (as opposed to diffuse)
SEGMENTAL—only part of an entire glomerulus is involved (as opposed to global) GLOMERULOSCLEROSIS—refers
to scarring of the glomerulus (a part of the nephron)
The important risk of intravenous drug use as a pathogenic factor of renal disease and shows a rarity of renal
disease in homosexual or bisexual men with AIDS.
The patient’s complaint matches the side effects of the Bactrim DS he is taking which is more common in AIDS
patients. This includes vomiting, nausea, urticaria, rashes and systemic lupus erythematous. There are no
significant findings in the urinalysis; amber colored urine may be due to his medications. If microscopic analysis is
performed, crystalluria may be observed as a side effect. If crystalluria is observed in the urinalysis, the patient will
experience irritation of the kidney. However, crystals observed in urinalysis are usually insignificant.
Kidney damage under a microscope showed diffuse glomerular membrane increased, with minimal glomerular
sclerosis. The number of occurrence ranging from segmental glomerular sclerosis, which is characterized by a thick
cytoplasm containing vacuoles of epithelial cell proliferation, capillary wall collapse, or because of protein
deposition (hyaline degradation) and to the capillaries disappear, cavity foam cells (lipid filled with mononuclear
cells). Glomerular cysts are usually expanded, tubular damage is extensive.
Focal Segmental Glomerulosclerosis (FSGS) is a disease that attacks the kidney’s filtering system (glomeruli)
causing serious scarring. FSGS is one of the many reasons of a disease known as Nephrotic Syndrome, which occurs
when valuable protein in the blood leaks into the urine (proteinuria).
V. REFERENCES
Susan King Strasinger, Urinalysis and Body Fluids, 2008
Amy M. Karch, Lippincott’s Nursing Drug Guide, 2009
http://www.drugs.com/sfx/bactrim-side-effects.html
www.medicinenet.com/abdominal_pain/article.htm
en.wikipedia.org/wiki/Abdominal_pain
http://www.medcohealth.com/medco/consumer/ehealth/ehsarticle.jsp?packageTemplate=HE+article+XML+templ
ate&ltSess=y&currentPage=%2Fconsumer%2Fehealth%2Fehsarticle.jsp&com.broadvision.session.new=Yes&article
ID=97666
en.wikipedia.org/wiki/Bowel_obstruction
www.answers.com/topic/ileus
www.health-care-clinic.com/family-health/i/ileus.htm
www.health-care-clinic.com/family-health/i/ileus.htm
http://en.wikipedia.org/wiki/Focal_segmental_glomerulosclerosis
http://www.ich.ucl.ac.uk/gosh_families/information_sheets/focal_segmental_glomerulosclerosis/image1.jpg
http://www.91sqs.com/attachments/2007/07/2446_200707141110261.jpg
http://www.nephcure.org/fsgs-facts.htm
http://www.tcmwell.com/TCM_News/hiv/The-performance-of-HIV-infection---Urinary-system.html

Angeles University Foundation

Angeles City
College of Allied Medical Professions
Medical Technology Department

Post Prelim Conference in Clinical Microscopy

Case 7
Submitted By:
GROUP 10
Torres, Chelzylyn M.
Bacani, Fernando,
Ocampo, Toni Jerico
Savellano, Lara Mikee

Submitted To:
Ms. Crizelda Liwanag, RMT
Mrs. Eloisa Q. Singian, RMT

7 January 2010

Angeles University Foundation

Angeles City

Group 7
Dimaun, Joy
Sandoval, Noel
Santos, Marjorie
Soliman, Lea

Case
Jessica is a 20-year old woman admitted to R/O appendicitis, pancreatitis, pyelonephritis, abdominal abscess, or
ruptured viscus. She came to the ER complaining of severe abdominal pain or what is called an “acute abdomen”.
Because she was 36 weeks’ (estimated) IUP, a low C-section was performed and the child was delivered. Her
appendix was found to be ruptured and it was removed at the same time. Blood cultures were positive for E.coli,
sensitive to Cefotan (cefotetan disodium) and to gentamicin, which she was given. The urinalysis, obtained two
days postsurgery, was as follows: glucose negative, bilirubin small; ketones 40 mg/dL; specific gravity 1.025; blood
negative; pH 6.5; protein 30 mg/dL; urobilinogen 1.0 EU/dL; nitrite negative; leucocyte esterase trace; color
orange; WBCs 5-10/hpf; RBCs 0-2/hpf; epithelial cells 1+/hpf; bacteria 1+/hpf; bacteria 1+; casts 1-5 granular.
Ictotest negative. C&S was not requested on this urine.
Questions:
1. What aspects of the urinalysis do you find significant?
Microorganisms (bacteria, trichomonads, yeast)
In health, the urinary tract is sterile; there will be no microorganisms seen in the urine sediment. Microorganisms
are usually reported as "none," "few," "moderate," or "many" present per high power field (HPF). Bacteria from the
surrounding skin can enter the urinary tract at the urethra and move up to the bladder, causing a urinary tract
infection (UTI).
Leukocyte esterase: Normally negative. Leukocytes are the white blood cells (or pus cells). This looks for white blood
cells by reacting with an enzyme in the white cells. White blood cells in the urine suggests a urinary tract infection.
WBC up to 5/HPF are commonly accepted as normal. Greater numbers (pyuria) generally indicate the presence of
an inflammatory process somewhere along the course of the urinary tract (or urogenital tract in voided specimens).
Granular casts almost always indicate significant renal disease. However, granular casts may be present in the
urine for a short time following strenuous exercise. Granular casts that contain fine granules may appear grey or
pale yellow in color. Granular casts that contain larger coarse granules are darker. These casts often appear black
because of the density of the granules.
2. What pathophysiologic aspects of this case are illustrated by the urine microscopic examination?

The acute pyelonephritis of the patient is the result of the bacterial invasion (e.coli) from the ruptured appendictis
of the patient

Appendicitis
Appendicitis is a condition characterized by inflammation of the appendix. Reginald Fitz first described
acute and chronic appendicitis in 1886, and it has been recognized as one of the most common causes of
severe acute abdominal pain worldwide.
Symptoms
Signs and symptoms of acute appendicitis can be classified into two types, typical and atypical. The typical history
includes pain starting centrally (periumbilical) before localizing to the right iliac fossa (the lower right side of the
abdomen); this is due to the poor localizing property of visceral nerves from the mid-gut, followed by the
involvement of somatic nerves as the inflammation progresses. The pain is usually associated with loss of appetite
and fever, although the latter isn't a necessary symptom. Nausea or vomiting may occur, as well as drowsiness and
malaise.
Atypical symptoms may include pain beginning and staying in the right iliac fossa, diarrhea and a more prolonged,
smoldering course. If an inflamed appendix lies in contact with the bladder, there is frequency of urination. With
post-ileal appendix, marked retching may occur. Tenesmus or "downward urge" (the feeling that a bowel
movement will relieve discomfort) is also experienced in some cases.
Causes
On the basis of experimental evidence, acute appendicitis seems to be the end result of a primary obstruction of
the appendix lumen. Once this obstruction occurs the appendix subsequently becomes filled with mucus and
swells, increasing pressures within the lumen and the walls of the appendix, resulting in thrombosis and occlusion
of the small vessels, and stasis of lymphatic flow. Rarely, spontaneous recovery can occur at this point. As the
former progresses, the appendix becomes ischemic and then necrotic. As bacteria begin to leak out through the
dying walls, pus forms within and around the appendix (suppuration). The end result of this cascade is appendiceal
rupture (a 'burst appendix') causing peritonitis, which may lead to septicemia and eventually death.
Pyelonephritis
Pyelonephritis is an ascending urinary tract infection that has reached the pyelum (pelvis) of the kidney (nephros in
Greek). If the infection is severe, the term "urosepsis" is used interchangeably (sepsis being a systemic
inflammatory response syndrome due to infection). It requires antibiotics as therapy, and treatment of any
underlying causes to prevent recurrence. It is a form of nephritis. It can also be called pyelitis.
Diagnosis
The presence of nitrite and leukocytes (white blood cells) on a urine dipstick test in patients with typical symptoms
are sufficient for the diagnosis of pyelonephritis, and are an indication for empirical treatment. Formal diagnosis is
with culture of the urine; blood cultures may be needed if the source of the infection is initially doubtful.
Causes
Most cases of "community-acquired" pyelonephritis are due to bowel organisms that enter the urinary tract.
Common organisms are E. coli (70-80%) and Enterococcus faecalis. Hospital-acquired infections may be due to
coliforms and enterococci, as well as other organisms uncommon in the community (e.g. Klebsiella spp.,
Pseudomonas aeruginosa). Most cases of pyelonephritis start off as lower urinary tract infections, mainly cystitis
and prostatitis.
Pathology
Acute pyelonephritis is an exudative purulent localized inflammation of the renal pelvis (collecting system) and
kidney. The renal parenchyma presents in the interstitium abscesses (suppurative necrosis), consisting in purulent
exudate (pus): neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils). Tubules are damaged
by exudate and may contain neutrophil casts. In the early stages, glomeruli and vessels are normal. Gross
pathology often reveals pathognomonic radiations of hemorrhage and suppuration through the renal pelvis to the
renal cortex. Chronic infections can result in fibrosis and scarring.
Sample Test Paper
It is an infection of the kidney, and the ureters, the ducts that carry the urine away from the kidney?
Appendicitis
Pyelonephritis
Kidney stone
NOTA
Exams and test for pyelonephritis?
Blood cultures
Urine culture
Both
nota
Medications for pyelonephritis?
amoxicillin
cephalosporin
Both
nota
The following are other possible complication of pyelonephritis, exept?
Kidney failure
perinephric abscess
Sepsis
nota
The following are symptoms of pyelonephritis except?
Back pain
Abdominal apin
Fatigue
aota
These are urination problems of pyelonephritis?
Blood in the urine
Cloudy or abnormal urine color
Increased urinary frequency or urgery
AOTA
What is the probable cause of acquiring pyelonephritis in this case?
E. coli
Staphylococcus
Both
NOTA
Positive results for pyelonephritis?
Leukocyte
Bacteria
Both
Nota
A positive bilirubin and urobilinogen may lead to?
liver damage
heart failure
convulsion
aota

Presence of WBC in the urine indicates what?

Infection
Heart problems
No need to worry
nota

References:
http://library.med.utah.edu/WebPath/TUTORIAL/URINE/URINE.html
http://en.wikipedia.org/wiki/Urinary_cast
http://en.wikipedia.org/wiki/Appendicitis
http://en.wikipedia.org/wiki/Pyelonephritis
CLINICAL MICROSCOPY
group 4

[Type the document title]

[Type the document subtitle]
Robin Christian G. Cao

Johanna Selina D. Lim

Jennie Q. Lingad

Anna Kamille C. Suyat

[Year]

[TYPE THE COMPANY ADDRESS]

 Group 4
Cao, Robin Christian G.
Lim, Johanna Selina D.
Lingad, Jennie Q.
Suyat, Anna Kamille C.
Case 6
With a medical history of HTN, IDDM and CHF, this 57-year old woman was attending a
social event until the early morning hours, had been walking around complaining of shortness of
breath, and suddenly collapsed with a blood-tinged discharge coming from her mouth. She
was rushed to the ER in a private car and on arrival was unresponsive to verbal or painful stimuli,
and showed agonal respirations with a weak radial pulse. The impression was respiratory arrest,
acute pulmonary edema, R/O MI. Subsequent laboratory work did not support the diagnosis of
acute MI, suggesting instead acute pulmonary edema. Her admission urinalysis produced the
following results:

Urinalysis Results

Physical Examination

Color Amber

Appearance Hazy

pH 5.5

Specific Gravity 1.010

Chemical Examination

Protein 100 mg/dL

Glucose 250 mg/dL

Bilirubin and Ketones Negative

Urobilinogen Normal

Nitrite and Leukocyte Esterase Negative

Microscopic Examination

White Blood Cell 20-50/hpf

Red Blood Cell 0-2/hpf

Epithelial Cell Few/hpf

Bacteria 1+/hpf

Casts TNTC granular/lpf

Blood Small

Questions:

What urinalysis results do you find significant?

What pathophysiology of this case is most closely related to the urinary sediment
findings?
Answers:
Significant Findings

o Color : Amber

o Protein :100 mg/dL

o Glucose : 250 mg/dL

o WBC : 20-50/hpf

o Bacteria :1+/hpf

o Cast :Granular TNTC/LPF

This is a case of pulmonary edema secondary to left sided heart failure base on the
patient signs and symptoms and history of IDDM, CHF and Hypertension.

Pathophysiology
o The decreased in cardiac output in heart failure patients results in an "unloading"
of high-pressure baroceptors in the left ventricle, carotid sinus, and aortic arch.
This unloading leads to the generation of afferent signals to the central nervous
system that stimulate cardioregulatory centers in the brain which stimulate the
release of anti-diuretic hormone from the posterior pituitary. Antidiuretic hormone
(ADH) is a powerful vasoconstrictor that increases the permeability of the renal
collecting ducts, leading to the reabsorption of free water. These afferent signals
to the CNS also activate efferent sympathetic nervous system pathways that
innervate the heart, kidney, peripheral vasculature, and skeletal muscles.
Sympathetic stimulation of the kidney leads to the release of renin, with a
resultant increase in the circulating levels of angiotensin II and aldosterone. The
activation of the renin-angiotensin-aldosterone system promotes salt and water
retention and leads to vasoconstriction of the peripheral vasculature, myocyte
hypertrophy, myocyte cell death, and myocardial fibrosis. While these
neurohormonal mechanisms facilitate short-term adaptation by maintaining
blood pressure, and hence perfusion to vital organs, these same neurohormonal
mechanisms are believed to contribute to end-organ changes in the heart and
the circulation, and to the excessive salt and water retention in advance heart
failure.
In summary the cause of the concentrated urine which causes the amber color is
the release of Anti-diuretic hormone by the posterior pituitary and the activation
of renin-angiotensin-aldosterone pathway which lead to water reabsorption.

Amber Urine
o Amber colored urine is normal in the presence of dehydration this is due to the
increase in the concentration of urobilinogen which is a pigment that gives the
urine its color. When a person is well hydrated this urobilinogen is diluted resulting
to a yellow or sometimes colorless color of the urine. In our case where there is no
presence of fluid loss (dehydration) the principle that cause the amber colored
urine is the same (that it is due to a concentrated urine) but the mechanism that
cause this is different (no fluid loss or dehydartion). This mechanism is best
explained with the understanding of the pathopysiology of heart failure (disease
of the patient)
Proteinuria
o The presence of proteinuria is caused by the hypertension that is caused by the
vasoconstricting effect of angiotensin II and sodium retention by the aldosterone.
Hypertension causes proteinuria by altering the glomeruli and post glomeruli
structure this is due to ischemia or direct damage to this structure because of the
increase in pressure. These changes in turn allow the protein to pass through
resulting to proteinuria.
Glucosuria
o Glucosuria is caused by the patient IDDM. Glucosuria occurs when the
concentration of glucose in the urine is greater in the amount of glucose that the
kidney can reabsorb back in the circulation.
Pyuria and Bacteria +1
 o Pyuria and bacteria +1 may signify urinary tract infection. Since the patient is a
female and has history of IDDM she is most prone to the development of UTI.

Granular Casts
o The presence of granular cast that is TNTC signify that this patient has a long
standing UTI. This is due to the fact that granular cast are found on patient with
pyelonephritis, viral infection, and chronic lead poisoning. Since the patient
doesn’t have history of viral infection and chronic lead poisoning the most
probable cause of the granular cast are pyelonephritis (type of UTI).
o Granular cast may also be pathologic or non pathologic. The origin of the
granules in nonpathologic conditions appears to be from the lysosomes excreted
by RTE cells during normal metabolism. Increased cellular metabolism occurring
during strenuous exercise accounts for the transient increase of granular casts. In
disease states, granules may represent disintegration of cellular casts and tubule
cells or protein aggregates filtered by the glomerulus.

Reference:
o Robbins and Cotrans Pathologic Basis of Disease 7th Edition
o Harrisons Principle of Internal Medicine 17 Edition
o Henry’s Clinical Diagnosis and Management by Laboratory methods 21st Edition
o Oxford handbook of Clinical diagnosis 1st Edition

Case #5:

An 82 year old woman with an history of HTN treated with Vasotec (enapril maleate), and of NIDDM, was
seen in the outpatient clinic complaining of a blister on her lower lip that she said she had been
developing slowly over a year. The blister was diagnosed as a mucocele (a mucus cyst), and an
appointment was made to have it biopsied and excised at a future date. In the course of her examination,
a routine urinalysis (without the microscopic) was requested and the urine was found to be significant for
nitrite positive; and leukocyte esterase moderate. The results prompted the request for a urine C&S. The
urine C&S subsequently indicated a colony greater than 100,000 CFU/ml with an identification of E. coli.

What aspect of the urine sediment do you find significant?

- Pus cells and bacteria (Caused the Nitrite and Leukocytes Esterase test in the urine to be
positive.)
There are certain types of bacteria (e.g. E. coli) which have the ability to reduce nitrate, a
normal constituent of urine, to nitrite, which does not normally appear in the urine.
Therefore, Nitrites in the urine can be an early warning that a urinary tract infection might
exist.
A positive LE test result is most frequently accompanied by the presence of bacteria.
The LE detects the presence of esterase in the granulocytic white blood cells
(neutrophils, eosinophils, and basophils) and monocytes. Neutrophils are the leukocytes
most frequently associated with bacterial infections.

What diagnosis would you give this case?

- Urinary tract infection
The presence of a single type of bacteria (E. coli) growing at high colony counts (greater
than 100,000 colony forming units (CFU)/ml) indicates a Urinary Tract Infection.

What type of treatment do you think this patient was given for the condition shown here
- Antibiotic therapy with the correct dosage relating to her age.

Antibiotic Age Route Dosage

Trimethoprim-Sulfamethoxazole Adult ORAL or IV 160 mg-800 mg/

(TMP-SMX 12 hours for 10 to 14 days
8 to 10 mg/kg/day

Nitrofurantoin (Furadantin, Adult ORAL 50 to 100 mg four times daily for

Macrodantin seven days

Amoxicillin Adult ORAL 250 mgs/ 8 hrs or 500 mgs/12

hours.

What results will be expected upon performing the microscopic examination of the patient's
urine?
- Urine microscopic exam will be, pus cells ranging from many to TNTC (too numerous to count)
and bacteria.

References:
http://www.labtestsonline.org/understanding/analytes/urine_culture/test.html

http://www.testsymptomsathome.com/TEC06.asp

http://adam.about.com/reports/000036_7.htm

http://kidney.niddk.nih.gov/kudiseases/pubs/utiadult/

http://adam.about.com/reports/000036_7.htm

http://www.labtestsonline.org/understanding/analytes/urine_culture/test.html

http://www.testsymptomsathome.com/TEC06.asp
http://kidney.niddk.nih.gov/kudiseases/pubs/utiadult/

http://www.drugs.com/mtm/sulfamethoxazole-and-trimethoprim.html

http://en.wikipedia.org/wiki/Nitrofurantoin

http://www.drugs.com/pdr/amoxicillin.html

http://www.rxlist.com/vasotec-drug.htm

Angeles University Foundation

College of Allied Medical Professions

Department of Medical Technology

In Partial Fulfillment of the requirement in

Clinical Microscopy

(Case Analysis)
 Submitted by:

Group 5

Garcia, Vixienne Geia

Natividad, Justine Lorenz

Nicdao, Jan Kevin

BSMT III-A

Submitted to:

Ms. Crizelda Liwanag

Submitted on:

January 7, 2010

Sample Test Paper:

1. NIDDM stands for:

a. Non-Identifiable Diabetes Mellitus
b. Non-Insulin Dependent Diabetes Mellitus
c. Non-Insulin Deficient Diabetes Mellitus
2. In the case, the old woman was complaining of a blister on her lower lip, which was later
diagnosed as a mucocele. A mucocele is a/an:
a. Allergy
b. Mucus cyst
c. Mole
3. An excision and a/an ____ were scheduled on a future date for the mucocele.
a. Chemotherapy
b. Biopsy
c. Aspiration
4. Which of the following was used to treat the patient’s history of HTN?
a. Vasotec
b. Amoxicillin
c. Nitrofurantoin
5. The significant results of the requested Routine Urinalysis is/are:
a. Leukocyte esterase (many); nitrite (+)
b. Leukocyte esterase (few); nitrite (-)
c. Leukocyte esterase (moderate); nitrite (+)
6. The results in #5 prompted for a/an:
a. C&S
b. Repeat test
c. None; the tests were sufficient in diagnosis
7. Women tend to have higher LE values due to:
 a. Vaginal contamination
b. Difference in sexual activity
c. Men and women have same range values
8. In the nitrite reaction, which is normally found in the urine?
a. Nitrite
b. Nitrate
c. Both
9. The C&S results indicated:
a. >100,000 CFU/ml of E.coli
b. <100,000 CFU/ml of E.coli
c. 100,000 CFU/ml of E.coli
10. The diagnosis of the case was:
a. HTN
b. UTI
c. NIDDM

Answer Key:

1. NIDDM stands for:

a. Non-Identifiable Diabetes Mellitus
b. Non-Insulin Dependent Diabetes Mellitus
c. Non-Insulin Deficient Diabetes Mellitus
2. In the case, the old woman was complaining of a blister on her lower lip, which was later
diagnosed as a mucocele. A mucocele is a/an:
a. Allergy
b. Mucus cyst
c. Mole
3. An excision and a/an ____ were scheduled on a future date for the mucocele.
a. Chemotherapy
b. Biopsy
c. Aspiration
4. Which of the following was used to treat the patient’s history of HTN?
a. Vasotec
b. Amoxicillin
c. Nitrofurantoin
5. The significant results of the requested Routine Urinalysis is/are:
a. Leukocyte esterase (many); nitrite (+)
b. Leukocyte esterase (few); nitrite (-)
c. Leukocyte esterase (moderate); nitrite (+)
6. The results in #5 prompted for a/an:
a. C&S
b. Repeat test
c. None; the tests were sufficient in diagnosis
7. Women tend to have higher LE values due to:
a. Vaginal contamination
b. Difference in sexual activity
c. Men and women have same range values
8. In the nitrite reaction, which is normally found in the urine?
a. Nitrite
 b. Nitrate
c. Both
9. The C&S results indicated:
a. >100,000 CFU/ml of E.coli
b. <100,000 CFU/ml of E.coli
c. 100,000 CFU/ml of E.coli
10. The diagnosis of the case was:
a. HTN
b. UTI
c. NIDDM

Research Information:

Hypertension is a chronic medical condition in which the blood pressure is elevated. It is also
referred to as high blood pressure or shortened to HT, HTN or HPN. The word "hypertension", by itself,
normally refers to systemic, arterial hypertension. Hypertension can be classified as either essential
(primary) or secondary. Essential or primary hypertension means that no medical cause can be found to
explain the raised blood pressure. It is common. About 90-95% of hypertension is essential hypertension.
Secondary hypertension indicates that the high blood pressure is a result of (i.e., secondary to) another
condition, such as kidney disease or tumours (adrenal adenoma or pheochromocytoma). Persistent
hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and
is a leading cause of chronic renal failure. Even moderate elevation of arterial blood pressure leads to
shortened life expectancy. At severely high pressures, defined as mean arterial pressures 50% or more
above average, a person can expect to live no more than a few years unless appropriately treated.
Beginning at a systolic pressure (which is peak pressure in the arteries, which occurs near the end of the
cardiac cycle when the ventricles are contracting) of 115 mmHg and diastolic pressure (which is minimum
pressure in the arteries, which occurs near the beginning of the cardiac cycle when the ventricles are
filled with blood) of 75 mmHg (commonly written as 115/75 mmHg), cardiovascular disease (CVD) risk
doubles for each increment of 20/10 mmHg.

VASOTEC® (Enalapril Maleate) is the maleate salt of enalapril, the ethyl ester of a long-acting
angiotensin converting enzyme inhibitor, enalaprilat. Enalapril maleate is chemically described as (S)-1-
[N-[1-(ethoxycarbonyl)-3-phenylpropyl]-L-alanyl]-L-proline, (Z)-2-butenedioate salt (1:1). Enalapril maleate
is a white to off-white, crystalline powder with a molecular weight of 492.53. It is sparingly soluble in
water, soluble in ethanol, and freely soluble in methanol. Enalapril is a pro-drug; following oral
administration, it is bioactivated by hydrolysis of the ethyl ester to enalaprilat, which is the active
angiotensin converting enzyme inhibitor. VASOTEC is indicated for the treatment of hypertension. It is
effective alone or in combination with other antihypertensive agents, especially thiazide-type diuretics.
The blood pressure lowering effects of VASOTEC and thiazides are approximately additive.

Diabetes mellitus type 2 or type 2 diabetes (formerly called non-insulin-dependent

diabetes mellitus (NIDDM), or adult-onset diabetes) is a disorder that is characterized by high blood
glucose in the context of insulin resistance and relative insulin deficiency. Traditionally considered a
disease of adults, type 2 diabetes is increasingly diagnosed in children in parallel to rising obesity rates
due to alterations in dietary patterns as well as in life styles during childhood. Unlike type 1 diabetes,
there is very little tendency toward ketoacidosis in type 2 diabetes, though it is not unknown. One effect
that can occur is nonketonic hyperglycemia which also is quite dangerous, though it must be treated very
differently. Complex and multifactorial metabolic changes very often lead to damage and function
impairment of many organs, most importantly the cardiovascular system in both types. This leads to
substantially increased morbidity and mortality in both type 1 and type 2 patients, but the two have quite
different origins and treatments despite the similarity in complications.

An oral mucocele, is a clinical term that refers to two related phenomena: mucus extravasation
phenomenon, and mucus retention cyst. The former is a swelling of connective tissue consisting of
collected mucin due to a ruptured salivary gland duct usually caused by local trauma, in the case of
mucus extravasation phenomenon, and an obstructed salivary duct in the case of a mucus retention cyst.
The mucocele is a bluish translucent color, and is more commonly found in children and young adults.

A urinary tract infection (UTI) is a bacterial infection that affects any part of the urinary tract.
The main causitive agent is Escherichia coli. Although urine contains a variety of fluids, salts, and waste
products, it usually does not have bacteria in it. When bacteria get into the bladder or kidney and multiply
in the urine, they cause a UTI. The most common type of UTI is a bladder infection which is also often
called cystitis. Another kind of UTI is a kidney infection, known as pyelonephritis, and is much more
serious. Although they cause discomfort, urinary tract infections can usually be quickly and easily treated
with a short course of antibiotics.

Angeles University Foundation

Angeles City, Pampanga

Clinical Microscopy

Case Study Analysis

Group 6
Alagdon, Edsel
Gomez, Paul Arvin
Laus, Abigail

BSMT 3-A

Ms. Crizelda Liwanag

January 7, 2010

Case 10:
A 32-year old woman with a long history of IDDM has been checking her blood sugar at home daily and
administering her own insulin. On a rainy Sunday night, she was admitted through the ER after 2 days of vomiting,
upper abdominal pain, and right jaw pain. Her admission diagnosis was Diabetic Ketoacidosis and dehydration.
The admission urinalysis (no microscopic) was significant for glucose >1000 mg/dL and ketones >80 mg/dL. Her
condition was resolved with fluid and electrolyte therapy and insulin drip.

Guide Questions and Answers:

1. What urinalysis results correlate with the diagnosis of DKA?

Color Colorless
Odor Strong, sweet smell
pH Decreased
Protein Increased
Glucose Increased
Specific Gravity Increased
Ketones Present

2. Explain.
The color of the urine appears to be diluted, but the specific gravity is high due to the increased glucose content.
Excretion of ketone bodies in the urine is responsible for the sweet smell of the urine. The production of ketone
bodies increases the acidic nature of the urine. The presence of sugar in the blood leads to its excretion in to urine.
Ketones in the urine mean the body is burning fat to get energy.
3. What results should be expected from the microscopic examination?
In patients with diabetes mellitus, fatty casts are observed during microscopic examination of the urine.

10-item Sample Test Paper:

1. The urinalysis was significant because of:
a. Increased amount of glucose
b. Decreased amount of ketones
c. Presence of low specific gravity
d. Increased pH
2. What sediment constituents may be seen from the microscopic examination?
a. RBC casts
b. WBC
c. Fatty casts
d. Bacteria
3. What may be the cause of the woman having diabetic ketoacidosis on her case?
a. Failure to administer insulin
b. High insulin intake
c. Drinking lots of electrolytes
d. Low glucose level
4. Which will show a correct urinalysis results for Diabetic ketoacidosis?
a. Odor – normal; pH – 7; protein – increased; glucose – normal; spec. gravity – normal; ketones – negative
b. Odor –strong sweet; pH – decreased; protein – increased; glucose –increased; spec. gravity –increased;
ketones - present
c. Odor – normal; pH – decreased; protein – increased; glucose –increased; spec. gravity – normal; ketones -
negative
d. Odor –foul; pH – decreased; protein – increased; glucose – increased; spec. gravity – normal; ketones -
negative
e.
5. In the patient’s case, insulin level is low with type 1 Diabetes. What is the other name for this type?
a. Insulin Sufficient Diabetes mellitus
b. Adequate insulin diabetes mellitus
c. Non-insulin dependent diabetes mellitus
d. Insulin dependent diabetes mellitus
6. The insulin level of the patient is low because of:
a. Excessive urination and sweating
b. Her immune system destroys some beta cells in the pancreas
c. Her kidney is swelling
d. High glucose level
7. What organ of the body is responsible for the insulin problem in type 1 diabetes?
a. Kidney
b. Pancreas
c. Spleen
d. gallbladder
8. In the absence of glucose, most cells use this to produce ATP for energy production:
a. Fatty acids
b. Sucrose
c. Protein
d. Cells don’t use energy at all
9. Fatty acid breakdown causes:
a. Bad cholesterol production
b. Release of glucose
c. Fatty acid accumulation
d. Ketone production and accumulation
10. It is a condition among Diabetes patients wherein insulin deficiency or resistance causes the pulling of
fluid body tissues leading to polyuria and dehydration
a. Hyperglucosemia
b. Polyuria
c. Hyperglycemia
d. Metabolic acidosis

Answer Key:
1. A
2. C
3. A
4. B
5. D
6. B
7. B
8. A
9. D
10. C

Pertinent Information:
Autoimmune diseases are diseases that occur because of the body’s immune system attacking its own cells and
rendering a function useless as is the case in diabetes. In diabetes, the killer T cells of the body attack the insulin
producing cells of the pancreas; thereby, shutting down the production of insulin. When the production of insulin
is affected, the body cannot control the amount of sugar in the blood and this sugar is even excreted in the urine.
The liver then starts to produce ketone bodies as a response to the low insulin level, which the body is fooled into
thinking that, it is because of a low intake of glucose. The production of ketone bodies then increases the acidic
nature of the blood, because ketones are created from fatty acids and the adipose stores in the liver. At a certain
pH level that indicates high acidity, the tissues of the body start to die and the breath of diabetes patient has a
sweet, alcoholic smell that emergency room doctors immediately recognize as the symptom of diabetic
ketoacidosis. This condition is potentially fatal if not treated on time.

The presence of sugar in the blood leads to its excretion into urine, which is due to the overloading of certain
binding proteins in the kidneys that send back glucose into the blood in normal circumstances. Urine that usually
contains glucose and sugars has a sweet, fruity smell. However it is an indication that you need to rush to the
emergency room before ketoacidosis occurs and a possible coma.
References:
Diabetes Mellitus: A Guide to Patient Care by Lippincott Williams and Wilkins
Nutrition and Diagnosis-related Care by Sylvia Escott-Stump
Urinalysis and Other Body Fluids by Susan King Strasinger
Handbook of Disease by Lippincott Williams and Wilkins
Principles of Anatomy and Physiology by Gerard Tortora

Angeles University Foundation

AY 2009 – 2010

Clinical Microscopy:
Case Study No. 3
Group 2
Garcia, Tiffany Verzil
Geronimo, Jerome
Nogoy, Princess May
Ramos, Jayson

BSMT 3 – A

Ms. Crizelda D. Liwanag/Eloisa Q. Singian

Instructors

January 7, 2010
Summary

Patient: Man, 46 years old

Urinalysis results: Blood Chemistry Results:

Bilirubin: large Total Bilirubin: 32.1 mg/dL (0-1.5)
Color: amber Conjugated Bilirubin 22.2 mg/dL (0-0.4)
Casts: granular, 1-5/lpf ALP: 299 U/L (37-107)
WBC: 1-5/hpf AST: 302 U/L (8-42)
Ictotest: positive ALT: 46 U/L (3-96)
LD: 272 U/L (100-190)
Total Protein: 4.9 g/dL (6.4-8.2)
Albumin: 2.1 m/dL (3.4-5.0)
Accompanied Signs and Symptoms:
Diarrhea (entire previous month)
Gas and Nausea (previous 3 wks)
Jaundice

Patient Diagnosis:
Liver Cirrhosis
Hepatocellular Carcinoma
Obstructive Jaundice

Guide Questions:

What urine results correlate with the diagnosis? Explain.

Color: amber
o The patient’s urine color is caused by the presence of the abnormal pigment Bilirubin due to the
blockage of the hepatic portal vein which carries the bile pigment to the GIT. The presence of this
pigment in the urine, significantly in an increased level coincides with the diagnosis of the
patient’s liver diseases such as that of jaundice, cirrhosis and hepatocellular carcinoma.

Ictotest: positive
o Indicates the presence of Bilirubin which is correlated with liver damage and jaundice. This test is
requested to further identify if the amber colored urine is caused by early stages of liver
diseases.

Bilirubin: large
o Bilirubin resulted in high level in the urinalysis result due to the damaged integrity of the liver
and the blockage of the porta of hepatis (the liver’s portal vein), thus, the blood containing the
pigment cannot reach the gastrointestinal tract. The patient, having been diagnosed to have liver
cirrhosis at first - which is the onset of his history of alcoholism, wherein the liver is injured due
to massive alcohol consumption by blocking the normal metabolism of protein, fats and
carbohydrates – and further became hepatocellular carcinoma due to malignancy and severe
damage of the liver cells is confirmed to possess these diseases.

How do the blood analyses correlate with this? Explain.

Total Bilirubin and Conjugated Bilirubin – high

o Due to the blocked portal vein of the patient, direct bilirubin aggregated, escaped from the liver,
and ended up in the blood. Increased direct bilirubin usually means that the liver is obstructed,
thus, correlated to hepatic carcinoma and jaundice.
o Total Bilirubin is also increased due to cirrhosis of the patient.
Liver Enzymes:

ALP: 299 U/L (37-107)

o Alkaline Phosphatase, high. Elevated ALP detects diseases involving the biliary system of our
body. Since the patient has a liver disease, this enzyme is expected to rise because of the damage
of the oragan’s cells. This marker is intended to be sensitive upon the deterioration of the liver’s
cells, as in cirrhosis and carcinoma, wherein it is leaked out in the blood.
o It is elevated due to the excessive alcohol consumption, which indicates shedding of the liver,
cirrhosis – the patient showed history of alcoholism.
 AST: 302 U/L (8-42) - high
o Aspartate Amino Transferase (Serum Glutamate Oxaloacetate Transferase) showed high level. As
a liver enzyme, it is increased in the blood due to its leakage from the destructed cells of the
liver. But, as an enzyme involved in other organs such as the heart, and skeletal muscles, it is
more sensitive than specific. Still, due to the dramatic increase of ALP, it is confirmed that its
increase is due to the lowering profile of the liver. Thus, correlating to the patient’s diagnosis of
jaundice and hepatocellular carcinoma.

ALT: 46 U/L (3-96)

o Alanine Amino Transferase is, by contrast, normally found largely in the liver. This is not to say
that it is exclusively located in liver, but that is where it is most concentrated, making it specific
than only sensitive. It is released into the bloodstream as the result of liver injury. It therefore
serves as a fairly specific indicator of liver status of the patient.

LD: 272 U/L (100-190)

o Isoenzyme Fractionation detects any LD increase in the serum. Since this enzyme is not that
correlated with most of the hepatic disorders, due to its sensitivity, there can be a strong
possibility of liver damage. As the patient’s liver disease in the case is already chronic, great
increase in LD suggests that the diagnosis is highly correlated with the result.

Total Protein and Albumin – low

o Value of the total protein decreases in the serum is due to the decrease in the level of albumin,
globulin or both. Albumin is low due to the damage in the patient’s liver, wherein the low values
indicate the poor capability of the organ to synthesize proteins due to the concluded hepatic
profile of the patient.

Pathophysiology:

In this case, a long term history of the patient signifies the outcome of the diagnosis. Due to severe alcohol abuse,
the liver develops a scar tissue that replaces normal parenchyma, blocking the portal flow of blood through the
organ and disturbing normal function. Thus, if the portal vein is clogged, the blood containing the pigment from
the disintegration of the hemoglobin will not be able to enter the ducts of the bile and will not be able to reach the
GIT, making it a single way directed to the urinary system producing darker color urine and pale colored stool. The
pigment that creates the amber color of the patient’s urine is known to be bilirubin, which is not considered a
normal constituent. Blockage of the portal vein will result to a pressure into the liver obstructing it and damaging
its cells, thus creating jaundice.
The patient’s alcohol abuse led to the prior diagnosis of cirrhosis and by then succeeded to hepatocellular
carcinoma during the onset of its malignancy. Since the liver is the main organ in damage, protein synthesis is
dysfunctional, thus lowering the total protein and albumin levels of the patient’s serum under blood chemistry
tests. Enzymes, as known to hasten the synthesis of the proteins intracellularly, due to the patient’s liver disease,
leak outside the bloodstream, thus increasing the levels of enzymes extracellularly.

Name: ______________________________ Date: _________ Score: ____________

1. Increased levels of _________ in the urine may be due to liver disease, such as cirrhosis.
 a. bilirubin
b. rbc
c. bacteria

2. The most abundant blood plasma protein and is produced in the liver. Low level of this protein in blood indicates
liver disease.

a. globin
b. albumin
c. fibrinogen

3. Patients with long history of alcoholism may develop ______________.

a. hepatitis
b. cirrhosis
c. jaundice

4. This type of test is requested to detect early stages of liver disease, such as hepatitis.

a. Ictotest
b. AST
c. ALP

5. What test is done to diagnose liver or bone disease?

a. ALT
b. ALP
c. AST

6. The amber color of the urine is due to the presence of ____________in the urine

a. wbc
b. cast
c. bilirubin

7. What causes the appearance of conjugated bilirubin in the urine?

a. disrupted hemoglobin degradation

b. liver damage
c. both

8. An enzyme found in high amounts in heart muscle and liver and skeletal muscle cells.
a. ALT
b. AST
c. ALP

9. This type of jaundice is caused by an interruption to the drainage of bile duct

a. pre hepatic
b. hepatic
c. post hepatic

10. Its presence helps to determine the cause of clinical jaundice

 a. globin
b. albumin
c. conjugated bilirubin
1. A
2. B
3. B
4. A
5. B
6. C
7. C
8. B
9. C
10. C

References:

Strasinger, Susan K. & Di Lorenzo, Marjorie S. Urinalysis and Body Fluids. 5th Edition. F.A. Davis Company,
Thailand. 2005
Calbreath, Donald. Clinical Chemistry
http://www.medicinenet.com/liver_blood_tests/page2.htm
http://www.nlm.nih.gov/medlineplus/ency/article/003470.htm
http://www.abcompany.com/docgolob/bloodchemistry.htm
http://www.labtestsonline.org/understanding/analytes/bilirubin/faq.html
http://digestive.niddk.nih.gov/ddiseases/pubs/cirrhosis/#cause http://en.wikipedia.org/wiki/Gamma-
glutamyl_transpeptidase
http://en.wikipedia.org/wiki/Cirrhosis
http://en.wikipedia.org/wiki/Jaundice#Post-hepatic
http://web2.airmail.net/uthman/lab_test.html

hoAngeles University Foundation

College of Allied Medical Professions

Department of Medical Technology

CASE ANALYSIS
Preliminary term

In partial fulfillment of the requirements in

Clinical Microscopy

Submitted to:
Ms. Crizelda D. Liwanag, RMT, MS

Submitted by:

Guevarra, Sonny
Mungcal, Lilibeth
Sarmiento, Norilie Mae
Tayag, Joseph John S.

Group # 8

Summary of the case

Case #8

A urine specimen is obtained from a 14-year-old boy with a history of a sore throat. Three weeks ago he was
cultured and treated for a streptococcal throat infection with a single intramuscular dose of penicillin. Two weeks
after his initial visit, he showed no abnormal physical findings; however, his urinalysis revealed microscopic
hematuria and he was told to rest. Currently he has weakness and anorexia. He woke up with a headache and
puffy eyelids and says his urine is dark and there is very little of it.

Urinalysis Results:

Physical Appearance :

color: red (red-brown)

clarity: cloudy

Chemical Screening :

pH 6.0
specific gravity 1.025
protein (strip) 300 mg/dL protein (SSA) 3+
blood large
nitrite negative
leukocyte esterase negative
glucose negative
ketones negative
bilirubin negative
urobilinogen 0.5 EU/dl
Microscopic:

red blood cells 10-25/hpf (dysmorphic forms present)

white blood cells 0-2/hpf
casts 2-5 red blood cell casts/lpf
crystals few amorphous urates

Guide Questions:

1. What urinalysis findings are abnormal or discrepant?

The negative result for leukocyte esterase and the positive result for white blood cells in the microscopic
examination give discrepant information. However, this result may be due to the sensitivity of the leukocyte
esterase test. The test requires at least 5 WBC/hpf in order to yield a positive result, whereas, the microscopic
examination reveals only 0-2 WBC/hpf.

2. What is the significance of dysmorphic red cells in the urine sediment of this patient?

Dysmorphic red blood cells are RBC’s that vary in size, have cellular protrusions and are fragmented. These
abnormal RBC’s are associated primarily with glomerular bleeding.

3. Proteinuria is an important indication of renal disease. Match the following protein tests
(a and b) with the proteins they measure.

a. Reagent strip test for protein?

b. Sulfosalicylic acid test for protein?

_a/b__ albumin
_b___ Tamm-Horsfall glycoprotein
_b__ plasma globulins
 4. What is the significance of red blood cell casts in this patient?

The presence of RBC casts in the urine is more specific. This condition shows bleeding within the nephron. RBC
casts are primarily associated with the damage of the glomerulus that allows the passage of the cells through the
glomerular membrane.

5. Why don't you see bacteria in the microscopic examination of the sediment in this patient?

Although there is a presence of white blood cells in the microscopic examination, there are no bacteria seen in the
urine. This may be a signal that the renal disease is not of bacterial etiology.

6. What is the likely diagnosis for this patient?

The physical signs and symptoms and the medical history of the patient, together with the findings of the
urinalysis, constitutes the likely diagnosis for the patient which is acute glomerulonephritis (specifically acute
poststreptococcal glomerulonephritis).

Sample Test Paper

1. What would be the likely cause of the cloudy urine specimen in the case?

a. Red Blood Cells

b. White blood Cells
c. Urinary crystals
d. Squamous Epithelial Cells

2. The following may cause dysmorphic Red Blood Cells except:

a. Strenuous exercise
b. Glomerular bleeding
c. Diabetes mellitus

3. To be considered as UTI, bacteria should be accompanied by:

a. WBC’s
b. RBC’s
c. Bacterial motility
d. Abnormal urinary crystals
4. RBC’s are sometimes confused with WBC’s, yeasts and oil droplets. What reagent would be likely used to
confirm microscopic hematuria and the dysmorphic RBC’s

a. Sternheimer-Malbin
b. 1% acetic acid
c. Hansel Stain
d. Prussian blue

5. What result in the urinalysis constitutes to glomerulonephritis?

a. Hematuria
b. RBC casts
c. Proteinuria
d. All of the above

6. Red blood cell casts are associated with:

a. Strenuous contact sports

b. Proteinuria
c. Dysmorphic RBC’s
d. Only B and C
e. All of the above

7. Post infection glomerulonephritis is associated by recent infection of:

a. Staphylococcus aureus
b. Streptococcus agalactiae
c. Streptococcus pyogenes
d. B and C
e. All of the above

8. The build up of these substances in the nephron after infection may trigger glomerulonephritis

a. Immune complexes
b. M protein
c. Streptococcus toxin
d. Penicillin given to the patient

9. In the patient’s urinalysis, why is there presence of white blood cells?

a. To fight bacterial infection

b. The white blood cells attack the substances which inflames the nephron after a recent infection and
are filtered after
c. They pass through the compromised glomerular membrane together with other particles because
d. The white blood cells are not reabsorbed back into the blood vessels from the tubules

10. The following produces esterases except

a. Trichomonas
 b. Lymphocytes
c. Histiocytes

Answer key
1. A
2. C
3. A
4. B
5. D
6. E
7. C
8. A
9. C
10. B

Pertinent Information

A urinalysis (or "UA") is an array of tests performed on urine and one of the most common methods of medical
diagnosis. Urinalysis has three phases namely; the physical, chemical and microscopic examination. The physical
examination includes the determination of the urine color and clarity of urine. In the chemical test, the reagent
strip is currently used because it provides simple and rapid means for performing chemical analysis on urine. Tests
include pH, glucose, protein, ketones, blood, bilirubin, leukocyte esterase, urobilinogen and specific gravity. The
last part of urinalysis, microscopic examination, deals with the determination of urinary sediments. These include
RBC’s, WBC’s epithelial cells, casts, bacteria, parasites, yeasts, crystals mucus, spermatozoa and artifacts.

Urinary findings in the case

Color and Clarity
The color of urine may range from colorless to black. These may indicate normal conditions, physical activity,
metabolic functions or pathologic conditions.
Urine color Possible Clinical Significance
Colorless Recent fluid consumption
Pale yellow Polyuria or Diabetes
Dark Yellow Concentrated Urine
Yellow green Bilirubin oxidized to biliverdin
Green Pseudomonas infection
Pink/Red Hematuria (RBC’s, hemoglobin and myoglobin)

Brown/Black Methemoglobin, Alkaptonuria, Melanin

Color and clarity are routinely determined at the same time. Clarity refers to the transparency of the urine
specimen. Freshly voided normal urine is usually clear.
Clarity Term
Clear No visible particulates, transparent
Hazy Few particulates
Cloudy Many particulates
Turbid Print cannot be seen through urine
Milky May precipitate or clotted

*Clinical Significance of the physical examination

The urine specimen is said to be red and cloudy. This may indicate hematuria with many particulates.

Protein
The presence of proteinuria is often associated with renal disease. Normal urine contains very little protein
(<10mg/dL or 100mg per 24hours) is excreted. These proteins are primarily low-molecular-weight serum proteins
that have been filtered by the glomerulus and proteins produced from the genitourinary tract. Albumin is the
major protein found in normal urine. Normal albumin content is low because majority is not filtered by the
glomerulus and the filtered albumin is reabsorbed back into the tubules. Other proteins may include
microglobulins, Tamm-horsfall protein and proteins from prostatic, seminal and vaginal secretions. Demonstration
of proteinuria does not always signify renal disease. Clinical proteinuria is indicated at >30mg/dL.

*Clinical Significance of the protein test in the case

The result of the test reveals a large amount of protein present in the blood. This condition may be
associated to a renal disease, giving the disability of the glomerulus and tubules to properly filter and reabsorb the
proteins

Blood
Macroscopically, blood may be seen in the urine by means of hematuria (cloudy red urine) or
hemoglobinuria (clear red urine). Any amount of blood greater than 5 cells per microliter of urine is significant. In
the chemical examination, the test for hemoglobin is the most reliable means for determining blood.
Hematuria is closely associated with the renal and genitorurinary disorders in which bleeding is the result
of trauma or damage to the organs of these systems. Common causes may include renal calculi, glomerular
diseases, tumors and pyelonephritis. On the other hand, hemoglobinuria results from the lysis of the red blood cell
in which hemoglobin is released. It may also be a result of intravascular hemolysis and the subsequent filtering of
hemoglobin through the glomerulus. Intravascular hemolysis is evident in urine without red blood cells.
Another type of protein which may produce a red pigment is myoglobin. Its presence in the urine,
myoglobinuria, is indicative of muscular destruction. Myoglobin is a heme containing protein found in the muscle
that may react positively with the reagent strip for blood. The diagnosis of myoglobinuria is also based on the
patient’s medical history and serum levels of certain enzymes.

*Clinical Significance of the blood test in the case

The test is required to confirm if the red pigment in blood is caused by blood itself. Other substances such
as beets may produce red urine similar to hematuria. Blood gave a large result in the chemical test signifying “true
hematuria”.
Leukocyte Esterase
The Leukocyte esterase test is a urine test for the presence of white blood cells and other abnormalities
associated with infection. White blood cells in the urine, accompanied by bacteria, usually indicate a urinary tract
infection. The leukocyte esterase (LE) test detects esterase, an enzyme released by white blood cells specifically
granulocytes and monocytes. Positive test results are clinically significant. The LE test is also used to screen for
gonorrhea and for amniotic fluid infections. The combination of the LE test with the urinary nitrite test provides an
excellent screen for establishing the presence of a urinary tract infection (UTI). Urine sample that tests positive for
both nitrite and leukocyte esterase should be cultured for pathogenic bacteria.
Normal values for leukocyte esterase are based on the microscopic examination of 0-5 per hpf. Women
tend to have a higher number than men because of vaginal contamination.

Microscopic Red Blood Cells and Red Blood Cell Casts

Red blood cells in the urine sediments appear as smooth, non-nucleated and bi-concave disks and are
reported as the average number seen per 10 hpfs. RBC’s shrink and may appear crenated in concentrated urine,
due to the loss of water. In dilute solutions, RBC’s may rupture releasing the hemoglobin.
Dysmorphic RBC’s have cellular protrusions and are fragmented. They are primarily associated with
glomerular bleeding. The number and appearance of dysmorphic RBC’s must also be considered because abnormal
urine concentration affects RBC appearance. Dysmorphic cells are also associated with strenuous exercise. The
presence of RBC’s in the urine is associated with glomerular membrane or vascular injury within the genitourinary
tract.
The presence of RBC casts in the urine specifically indicates bleeding within the nephron. RBC casts are
associated with glomerulonephritis that allow the passage the passage of cells through the glomerular membrane.
RBC casts associated with glomerular damage are usually accompanied by proteinuria and dysmorphic RBC’s. Like
dysmorphic cells, RBC cast formation may be triggered by strenuous activities. RBC casts should be accompanied
by free standing RBC to prevent inaccurate reporting or misidentification of the casts.

White Blood Cells

WBC’s are slightly larger than RBC’s. The predominant WBC found in urine sediment is the neutrophil.
Neutrophils exposed to hypotonic urine absorb water and swell. Brownian movement of the granules within these
cells produces a sparkling appearance known as glitter cells. Presence of eosinophils upon staining indicates drug
induced interstitial nephritis, UTI and renal transplant rejection.
Pyuria (increase in urinary WBC indicates the presence of inflammation in the genitourinary system. Examples of
bacterial infections are pyelonephritis, cystitis, and prostatitis. Pyuria may also be present in nonbacterial disorders
such as glomerulonephritis, lupus erythemathosus and tumors.

Amorphous Urates
Amorphous urates are microspically yellow brown granules and are normal crystals seen in acidic urine.
They occur in clumps that may resemble casts.

Acute Glomerulonephritis
Acute glomerulonephritis is characterized by the sudden appearance of hematuria, proteinuria and red blood cell
casts in the urine, edema (most noticeable around the eyes), fatigue and hypertension with or without oliguria. It
can follow streptococcal infections. This illness was first recognized as a complication of the convalescence period
of scarlet fever in the 18th century. A link between hemolytic streptococci (group A and contains the M protein in
the cell wall) and acute glomerulonephritis was recognized in the 20th century.

Pathophysiology
Poststreptococcal glomerulonephritis follows infection with only certain strains of streptococci, designated as
nephritogenic. The offending organisms are virtually always group A streptococci. Acute poststreptococcal
glomerulonephritis (APSGN) follows pyodermatitis with streptococci M types 47, 49, 55, 2, 60, and 57 and throat
infection with streptococci M types 1, 2, 4, 3, 25, 49, and 12.
APSGN is believed to be an immune-mediated disease, in which an immune complex containing a streptococcal
antigen is deposited in the affected glomeruli. The size of glomerular basement membrane (GBM) pores and the
molecular size of the streptococcus-Ig complex are also important determinants. The molecular size of the
streptococcus-Ig complex is about 15 nm (10 nm for streptococcus group A and 5 nm for immunoglobulin). The
GBM pore sizes in children and adults are 2-3 nm and 4-4.5 nm, respectively. Therefore, the immune complex
molecule can be more easily rodded into the glomerulus in children than in adults and, thus, may explain the
increased frequency of APSGN in children compared to that in adults.
Successful management of the secondary complications, until the immune complexes have been cleared
from the blood will result in no permanent kidney damage.

References:
S. K. Strasinger and M.S. Di Lorenzo, Urinalysis and Body Fluids, 4 th ed., 2001
http://emedicine.medscape.com/article/777272-overview
http://emedicine.medscape.com/article/240337-overview
http://en.wikipedia.org/wiki/Glomerulonephritis
http://library.med.utah.edu/WebPath/TUTORIAL/URINE/URINE.html
http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cm&part=A5435
http://medres.med.ucla.edu/Education/Lectures_and_Conferences/IMS_2007_pdf/CCJM%20Proteinuria%202003.
pdf